• Ivo A van der Bilt, Djo Hasan, Renee B van den Brink, Maarten J Cramer, Mathieu van der Jagt, Fop van Kooten, Joost G Regtien, Maarten P van den Berg, Rob J Groen, Folkert J Ten Cate, Otto Kamp, Marco J Götte, Janneke Horn, Armand R Girbes, W Peter Vandertop, Ale Algra, Gabriel J Rinkel, Arthur A Wilde, and SEASAH (Serial Echocardiography After Subarachnoid Hemorrhage) Investigators.
• *Heart Center, Department of Clinical and Experimental Cardiology, Academic Medical Center, Amsterdam; ‡Department of Cardiology, University Medical Center, Utrecht; §Department of Intensive Care, Erasmus Medical Center, Rotterdam; ¶Department of Neurology, Erasmus Medical Center, Rotterdam; ‖Department of Intensive Care, University Medical Center, Groningen; #Department of Cardiology, University Medical Center, Groningen; **Department of Neurosurgery, University Medical Center, Groningen; ‡‡Department of Cardiology, Erasmus Medical Center, Rotterdam; §§Department of Cardiology, VU University Medical Center; ¶¶Department of Cardiology, Haga Teaching Hospital the Hague; ‖‖Department of Intensive Care, Academic Medical Center, Amsterdam; ##Department of Intensive Care, VU University Medical Center; ***Neurosurgical Center Amsterdam at Academic Medical Center and VU University Medical Center, Amsterdam; ‡‡‡Department of Clinical Epidemiology, Julius Center for Health Sciences and Primary Care, Utrecht; §§§Departments of Neurology and Neurosurgery, Brain Center Rudolf Magnus, University Medical Center, Utrecht, the Netherlands.
• Neurosurgery. 2015 Jun 1; 76 (6): 700-5; discussion 705-6.

BackgroundMyocardial wall motion abnormalities (WMAs) are independent risk factors for a poor outcome in patients with aneurysmal subarachnoid hemorrhage (aSAH).ObjectiveTo study the time course of WMAs during the initial phase after aSAH and to investigate which clinical, electrocardiographic, or myocardial serum markers are predictors of early or late development of WMAs.MethodsIn a prospective, multicenter cohort study in patients with aSAH, we performed serial electrocardiography and echocardiography and measured troponin T and N-terminal pro-B-type natriuretic peptide. WMAs present on admission were considered early WMAs; those that developed during the clinical course were considered late WMAs. Using multivariable regression analysis, we calculated odds ratios with corresponding 95% confidence intervals for clinical parameters, electrocardiography, and myocardial serum makers with early or late occurrence of WMAs.ResultsWe included 301 patients (mean age ± SD, 57 ± 13) years. Multivariable odds ratios for early WMAs were poor clinical condition, 2.7 (95% confidence interval: 1.1-6.8); sinus tachycardia, 5.0 (1.3-19.9); ST-segment depression, 3.7 (1.02-13.1); ST-segment elevation, 16.6 (1.5-178.9); and increased troponin T, 2.8 (1.1-7.3). Multivariable odds ratios (95% confidence intervals) for late development of WMAs were 6.8 (1.6-30) for a myocardial infarct pattern on admission electrocardiography and 3.4 (1.4-8.5) for increased troponin T on admission.ConclusionWMAs may be present on admission or develop during the course of aSAH. Poor neurological condition on admission, sinus tachycardia, ST-segment depression, and ST-segment elevation on admission electrocardiography and increased troponin T are independent predictors of early WMAs; a myocardial infarct pattern on admission ECG and increased troponin T independently predict late WMAs.Clinical Trial RegistrationNCT00123695.

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